不同时期COPD患者血清DcR3、Survivin表达水平及临床意义

目的 探讨不同时期慢性阻塞性肺疾病(COPD)患者血清诱饵受体3(DcR3)、凋亡抑制蛋白(Survivin)表达水平及临床意义。方法 选取2018年9月—2019年12月本院收治的92名COPD患者为研究对象,其中稳定型COPD 50例,急性加重期COPD 42例;同期本院健康体检者88例为对照组。测定各组研究对象血清DcR3、Survivin水平及肺功能指标。 与对照组[DcR3(106.54±48.35)pg/mL,Survivin(98.85±26.59)pg/mL]比较,稳定期组和急性加重期组血清DcR3[(395.23±123.85)pg/mL,(1 248.81±213.59)pg/mL]、Survivin [(267.54±84.69)pg/mL,(1 233.95±307.26)pg/mL]水平升高;与稳定期组比较,急性加重期组血清DcR3、Survivin水平升高。与对照组比较,稳定期组和急性加重期组FEV1%、FEV1 /FVC、DLCO%水平降低(P<0.001);与稳定期组比较,急性加重期组FEV1%、FEV1 /FVC、DLCO%水平降低(P<0.001)。随着低氧血症严重程度的增加,COPD患者血清DcR3、Survivin水平逐渐增加(P<0.001)。多因素logistics回归分析显示,高水平DcR3、Survivin、IL-12、hs-CRP为COPD病情的危险因素(P<0.001)。DcR3、Survivin与FEV、FEV1 /FVC呈负相关,与IL-12、TNF-α、hs-CRP呈正相关(P<0.001)。 COPD稳定期、急性加重期患者血清DcR3、Survivin表达水平升高,且DcR3、Survivin与COPD病情严重程度呈正相关。     

Practice developments supporting change implementation in Wellington,New Zealand (NZ) for ‘continuity of care when transitioning complex preterm infants from NICU to home’

The discussion paper will focus on continuity of care relating to previous NZ research, specifically to transitioning complex preterm infants from NICU to home based on parent experiences, and on the practice developments that have occurred, to ensure optimal health outcomes. Previous NZ research discovered parent desire a consistent service delivery for the entire transition journey from NICU and at home.An informative and comprehensive opportunity has occurred for reflective professional practice, evaluation, development and implementation which have transpired in positive change through innovative practice developments and support change implementation in Wellington, NZ. This has resulted in the articulation of a model of care that has both embraced and integrated parental desires for a continuity of care process for complex preterm infants. This has been achieved by having the same Discharge Facilitator/Key Case Manager present within the NICU and external to the NICU for Home-based infants for the entire transition journey.The paper will focus and emphasis additional practice development changes and furthermore, will present a real purpose, for other countries to learn of such practice developments that have exemplified a celebratory success for families of Wellington, NZ.     

Diabetic macular ischaemia- a new therapeutic target?

Diabetic macular ischaemia (DMI) is traditionally defined and graded based on the angiographic evidence of an enlarged and irregular foveal avascular zone. However, these anatomical changes are not surrogate markers for visual impairment. We postulate that there are vascular phenotypes of DMI based on the relative perfusion deficits of various retinal capillary plexuses and choriocapillaris. This review highlights several mechanistic pathways, including the role of hypoxia and the complex relation between neurons, glia, and microvasculature. The current animal models are reviewed, with shortcomings noted. Therefore, utilising the advancing technology of optical coherence tomography angiography (OCTA) to identify the reversible DMI phenotypes may be the key to successful therapeutic interventions for DMI. However, there is a need to standardise the nomenclature of OCTA perfusion status. Visual acuity is not an ideal endpoint for DMI clinical trials. New trial endpoints that represent disease progression need to be developed before irreversible vision loss in patients with DMI. Natural history studies are required to determine the course of each vascular and neuronal parameter to define the DMI phenotypes. These DMI phenotypes may also partly explain the development and recurrence of diabetic macular oedema. It is also currently unclear where and how DMI fits into the diabetic retinopathy severity scales, further highlighting the need to better define the progression of diabetic retinopathy and DMI based on both multimodal imaging and visual function. Finally, we discuss a complete set of proposed therapeutic pathways for DMI, including cell-based therapies that may provide restorative potential.     

Intervention rates and outcomes in medically managed uncomplicated descending thoracic aortic dissections

ObjectiveTo evaluate the long-term incidence and outcome of aortic interventions for medically managed uncomplicated thoracic aortic dissections.MethodsBetween January 2012 and December 2018, 91 patients were discharged home with an uncomplicated, medically treated aortic dissection (involving the descending aorta with or without aortic arch involvement, no ascending involvement). After a median period of 4 (first quartile: 2, third quartile: 11) months, 30 patients (33%) required an aortic intervention. Patient characteristics, radiographic, treatment, and follow-up data were compared for patients with and without aortic interventions. A competing risk regression model was analyzed to identify independent predictors of aortic intervention and to predict the risk for intervention.ResultsPatients who underwent aortic interventions had significantly larger thoracic (P = .041) and abdominal (P = .015) aortic diameters, the dissection was significantly longer (P = .035), there were more communications between both lumina (P = .040), and the first communication was significantly closer to the left subclavian artery (P = .049). A descending thoracic aortic diameter exceeding 45 mm was predictive for an aortic intervention (P = .001; subdistribution hazard ratio: 3.51). The risk for aortic intervention was 27% ± 10% and 36% ± 11% after 1 and 3 years, respectively. Fourteen patients (47%) underwent thoracic endovascular aortic repair, 11 patients (37%) thoracic endovascular aortic repair and left carotid to subclavian bypass, 3 patients (10%) total arch replacement with the frozen elephant trunk technique, and 2 patients (7%) thoracoabdominal aortic replacement. We observed no in-hospital mortality.ConclusionsThe need for secondary aortic interventions in patients with initially medically managed, uncomplicated descending aortic dissections is substantial. The full spectrum of aortic treatment options (endovascular, hybrid, conventional open surgical) is required in these patients.     

How does transfusion-associated graft-versus-host disease compare to hematopoietic cell transplantation-associated graft-versus-host disease?

Transfusion-associated graft-versus-host disease (TA-GVHD) is a rare life-threatening complication of blood transfusion caused by donor T cells that escape rejection by the recipient immune system. These donor T cells drive recipient tissue damage in response to host antigens. On the other hand, GVHD occurring after allogeneic hematopoietic cell transplantation (HCT-GVHD) is also caused by donor T cells, but its pathophysiology is more complex and differs due to the effects of tissue damage caused by pre?HCT conditioning and profound immunosuppression. Both TA-GVHD and HCT-GVHD can be fatal; however, mortality is higher with TA-GVHD due to the paucity of treatment options. Here, we compare and summarize the presentation, diagnosis, pathophysiology, prevention, and treatment of TA-GVHD and HCT-GVHD.     

Brilliance型16排螺旋CT的故障分析与维修

针对日常使用中遇到的Brilliance 16排螺旋CT高压系统、机架以及控制器局域网络(CAN)通讯等故障现象进行分析与维修,最终通过更换滤波电容、机架数据采集控制器(DMC)电源以及信号刷等配件得以排除故障。通过对故障准确判断以及合理运用厂家Service模式下的维修工具软件快速解决故障,保障了影像科检查工作的顺利进行,从而提高设备的稳定性。